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Carbon Monoxide Poisoning
Aka: Carbon Monoxide Poisoning, Carbon Monoxide- See Also
- Epidemiology
- Leading cause of toxin related death in United States
- Sources: Carbon Monoxide
- Gas powered engine
- Car with faulty exhaust system
- Passengers riding in back of a pickup truck
- Swimmers at back of a houseboat
- Propane fueled forklifts
- Ice skating rink Zamboni
- Indoor tractor pulls
- Home
- Indoor Heaters (most common cause)
- Furnace
- Home water heaters
- Gas heaters
- Pool heaters
- Kerosene heaters
- Indoor Flames
- Wood stoves
- Indoor charcoal fires
- Sterno fuel
- Tobacco smoke
- Tobacco Smokers
- Carboxyhemoglobin levels may reach 6-10%
- Hookah Smokers
- Carboxyhemoglobin levels may reach 15-20%
- Nonsmokers exposed to passive smoke
- Cigarette tip 2.5 fold greater CO than inhaled
- Tobacco Smokers
- Indoor Heaters (most common cause)
- Industrial or Occupational
- Steel foundry
- Pulp paper mill
- Formaldehyde and coke producing plants
- Fire fighters
- Fire
- Building or structure fire
- Wilderness fire
- Gas powered engine
- Pathophysiology
- Carbon Monoxide Properties (no warning features that gas is present until symptoms develop)
- Colorless
- Odorless
- Non-irritating gas
- Small molecule that crosses through some barriers into closed spaces (e.g. drywall)
- Exposures leading to Toxicity
- Carbon Monoxide toxicity occurs at Ambient levels >200-500 parts per million
- More severe illness occurs with longer exposure times
- Carbon Monoxide inhalation
- Carbon Monoxide has a high affinity for Hemoglobin (>200-250 times higher affinity than oxygen)
- Displaces Oxygen and produces Carboxyhemoglobin
- Shifts oxygen dissociation curve left with poor delivery of any residual oxygen to tissues
- Functional Anemia is however not responsible for Carbon Monoxide's lethal effects
- Direct toxin effects of Carbon Monoxide
- Sodium channel activation
- Nitric oxide levels increase
- Neurotoxic
- Basal Ganglia (Parkinsonism)
- Occiput (occipital blindness)
- Frontal cortex (personality change)
- Inflammatory cascade (responsible for neurologic toxicity)
- White Blood Cell response
- Glutamic acid (inflammatory)
- Free radicals
- Carbon Monoxide Properties (no warning features that gas is present until symptoms develop)
- History
- Multiple persons (e.g. family, coworkers, pets) in the same environment with similar symptoms
- Symptoms
- Headache (88%)
- Dizziness (83%)
- Nausea (75%)
- Drowsiness (75%)
- Dry Mouth (44%)
- Syncope
- Chest Pain
- Shortness of Breath
- Myalgias
- Carbon Monoxide also binds myoglobin
- Signs
- Cherry-red skin and mucosa
- Late or post-mortem finding
- Bounding Pulse
- Hypertension
- Muscular fasciculations
- Stertorous breathing
- Dilated pupils
- Convulsions
- Altered Mental State to coma
- Do not rely on Oxygen Saturations (not accurate see below)
- Cherry-red skin and mucosa
- Findings: Carboxyhemoglobin level
- Carboxyhemoglobin: 10%
- Frontal Headache
- Carboxyhemoglobin: 20%
- Carboxyhemoglobin: 30%
- Carboxyhemoglobin: 40%
- Confusion
- Syncope
- Carboxyhemoglobin: 50%
- Carboxyhemoglobin: 60%
- Carboxyhemoglobin: 70%
- Death
- Carboxyhemoglobin: 10%
- Labs
- Blood grossly appears abnormal red color
- Venous Blood Gas
- Carboxyhemoglobin
- Normal background Carboxyhemoglobin is 2-3%
- Carboxyhemoglobin elevated >25% is significant and associated with toxicity
- See above for findings related to Carboxyhemoglobin levels
- Complete Blood Count
- Precautions
- Oxygen Saturation (Pulse Oximeter) data is inaccurate
- Does not distinguish Carboxyhemoglobin from oxygenated Hemoglobin
- Drywall does not deter Carbon Monoxide
- Carbon Monoxide diffuses across drywall and may permeate separated rooms in multi-tenant housing
- Consider concurrent Cyanide toxicity in structure fires
- Smoke Inhalation and Lactic Acid >8 suggests cyanide Poisoning
- Especially with Altered Level of Consciousness
- Start oxygen while awaiting lab testing results if higher level of suspicion
- Start 100% oxygen via non-rebreather
- Hyperglycemia is a Neurotoxin and worsens outcomes
- Oxygen Saturation (Pulse Oximeter) data is inaccurate
- Management: Mild Poisoning
- Criteria
- Carboxyhemoglobin <30%
- No Neurologic or Cardiovascular Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5%
- Carbon Monoxide decreases 50% in 6 hours on room air
- Carbon Monoxide decreases 50% in 60 minutes on Non-Rebreather Mask
- Carbon Monoxide decreases 50% in 30 minutes on 100% oxygen while intubated
- Continuous Positive Airway Pressure (CPAP) with oxygen lowers Carbon Monoxide faster than oxygen alone
- Admission criteria
- All patients with Carboxyhemoglobin >25%
- Underlying heart disease
- Oxygen 100% Non-Rebreathing Mask
- Criteria
- Management: Moderate Poisoning
- Criteria
- Carboxyhemoglobin: 30-40%
- No Neurologic Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5% (see above)
- Admission to telemetry (cardiovascular monitor)
- Consider hyperbaric oxygen (see below)
- Cerebellar signs
- Focal neurologic deficit
- Persistent severe Headache
- Loss of consciousness, Seizure or coma
- Glasgow Coma Scale (GCS) <15
- Age >36 years old
- Prolonged Carbon Monoxide exposure
- Venous Blood Gas
- Determine acid-base status
- Oxygen 100% Non-Rebreathing Mask
- Criteria
- Management: Severe Poisoning
- Criteria
- Carboxyhemoglobin: >40%
- Neurologic Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5% (see above)
- Admission to telemetry (cardiovascular monitor)
- Endotracheal Intubation may be required due to severe Hypoxemia
- Venous Blood Gas
- Follow acid-base status
- Extracorporeal Membrane Oxygenation (VA-ECMO)
- Indicated in refractory cardiovascular collapse
- Hyperbaric oxygen chamber
- Mechanism
- Carbon Monoxide decreases 50% in 20-30 minutes on hyperbaric oxygen at 2.8 atm
- Allows oxygen to dissolve in blood at a much greater extent (beyond Hemoglobin binding)
- Decreases inflammatory cascade
- Decreases reperfusion injury
- Efficacy
- Decreases risk of delayed neuropsychiatric effects
- Reduces risk of personality change, Parkinsonism, cognitive effects
- Better short-term and long-term cognitive outcome
- Weaver (2002) N Engl J Med 347:1057-67 [PubMed]
- Decreases risk of delayed neuropsychiatric effects
- Criteria
- Ideally performed within 6 hours of presentation
- Chamber immediately available OR
- No improvement in 4 hours
- Cardiovascular status
- Neurologic status
- Mechanism
- Oxygen 100% Non-Rebreathing Mask
- Criteria
- Complications
- Hypoxic Encephalopathy
- Cognitive effects may persist for weeks to months or even permanently
- Parkinsonism
- Occipital blindness
- Personality change
- Coronary ischemia or myocadial infarction
- Increased risk of Coronary Artery Disease
- Hypoxic Encephalopathy
- Prevention
- Resources
- Consumer Products Safety Commission
- References
- Moayedi and Swaminathan in Herbert (2016) EM:Rap 16(7): 13-14
- Nordt and Shoenberger in Herbert (2019) EM:Rap 19(1): 4-6
- Reisdorf (1996) in Tintinelli (1996)
- (1995) MMWR Morb Mortal Wkly Rep 44:765-7 [PubMed]